Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels
Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces...
Ausführliche Beschreibung
Autor*in: |
Otis, Jessica P. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2017 |
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Anmerkung: |
© Springer-Verlag Berlin Heidelberg 2017 |
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Übergeordnetes Werk: |
Enthalten in: Journal of comparative physiology - Berlin : Springer, 1984, 187(2017), 4 vom: 31. Jan., Seite 639-648 |
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Übergeordnetes Werk: |
volume:187 ; year:2017 ; number:4 ; day:31 ; month:01 ; pages:639-648 |
Links: |
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DOI / URN: |
10.1007/s00360-017-1056-y |
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Katalog-ID: |
SPR004493176 |
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520 | |a Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. | ||
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700 | 1 | |a Pike, Amanda C. |4 aut | |
700 | 1 | |a Torrealba, Jose R. |4 aut | |
700 | 1 | |a Carey, Hannah V. |4 aut | |
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10.1007/s00360-017-1056-y doi (DE-627)SPR004493176 (SPR)s00360-017-1056-y-e DE-627 ger DE-627 rakwb eng Otis, Jessica P. verfasserin aut Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2017 Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 Pike, Amanda C. aut Torrealba, Jose R. aut Carey, Hannah V. aut Enthalten in Journal of comparative physiology Berlin : Springer, 1984 187(2017), 4 vom: 31. Jan., Seite 639-648 (DE-627)25376968X (DE-600)1459302-6 1432-136X nnns volume:187 year:2017 number:4 day:31 month:01 pages:639-648 https://dx.doi.org/10.1007/s00360-017-1056-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 187 2017 4 31 01 639-648 |
spelling |
10.1007/s00360-017-1056-y doi (DE-627)SPR004493176 (SPR)s00360-017-1056-y-e DE-627 ger DE-627 rakwb eng Otis, Jessica P. verfasserin aut Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2017 Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 Pike, Amanda C. aut Torrealba, Jose R. aut Carey, Hannah V. aut Enthalten in Journal of comparative physiology Berlin : Springer, 1984 187(2017), 4 vom: 31. Jan., Seite 639-648 (DE-627)25376968X (DE-600)1459302-6 1432-136X nnns volume:187 year:2017 number:4 day:31 month:01 pages:639-648 https://dx.doi.org/10.1007/s00360-017-1056-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 187 2017 4 31 01 639-648 |
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10.1007/s00360-017-1056-y doi (DE-627)SPR004493176 (SPR)s00360-017-1056-y-e DE-627 ger DE-627 rakwb eng Otis, Jessica P. verfasserin aut Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2017 Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 Pike, Amanda C. aut Torrealba, Jose R. aut Carey, Hannah V. aut Enthalten in Journal of comparative physiology Berlin : Springer, 1984 187(2017), 4 vom: 31. Jan., Seite 639-648 (DE-627)25376968X (DE-600)1459302-6 1432-136X nnns volume:187 year:2017 number:4 day:31 month:01 pages:639-648 https://dx.doi.org/10.1007/s00360-017-1056-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 187 2017 4 31 01 639-648 |
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10.1007/s00360-017-1056-y doi (DE-627)SPR004493176 (SPR)s00360-017-1056-y-e DE-627 ger DE-627 rakwb eng Otis, Jessica P. verfasserin aut Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2017 Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 Pike, Amanda C. aut Torrealba, Jose R. aut Carey, Hannah V. aut Enthalten in Journal of comparative physiology Berlin : Springer, 1984 187(2017), 4 vom: 31. Jan., Seite 639-648 (DE-627)25376968X (DE-600)1459302-6 1432-136X nnns volume:187 year:2017 number:4 day:31 month:01 pages:639-648 https://dx.doi.org/10.1007/s00360-017-1056-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 187 2017 4 31 01 639-648 |
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10.1007/s00360-017-1056-y doi (DE-627)SPR004493176 (SPR)s00360-017-1056-y-e DE-627 ger DE-627 rakwb eng Otis, Jessica P. verfasserin aut Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2017 Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 Pike, Amanda C. aut Torrealba, Jose R. aut Carey, Hannah V. aut Enthalten in Journal of comparative physiology Berlin : Springer, 1984 187(2017), 4 vom: 31. Jan., Seite 639-648 (DE-627)25376968X (DE-600)1459302-6 1432-136X nnns volume:187 year:2017 number:4 day:31 month:01 pages:639-648 https://dx.doi.org/10.1007/s00360-017-1056-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_381 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 187 2017 4 31 01 639-648 |
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Otis, Jessica P. @@aut@@ Pike, Amanda C. @@aut@@ Torrealba, Jose R. @@aut@@ Carey, Hannah V. @@aut@@ |
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Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Torpor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Hepatocyte</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Inosine</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Biliverdin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Preconditioining</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pike, Amanda C.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Torrealba, Jose R.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Carey, Hannah V.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of comparative physiology</subfield><subfield code="d">Berlin : Springer, 1984</subfield><subfield code="g">187(2017), 4 vom: 31. 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Otis, Jessica P. |
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Otis, Jessica P. misc Torpor misc Hepatocyte misc Inosine misc Biliverdin misc Preconditioining Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
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1432-136X |
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Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels Torpor (dpeaa)DE-He213 Hepatocyte (dpeaa)DE-He213 Inosine (dpeaa)DE-He213 Biliverdin (dpeaa)DE-He213 Preconditioining (dpeaa)DE-He213 |
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misc Torpor misc Hepatocyte misc Inosine misc Biliverdin misc Preconditioining |
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misc Torpor misc Hepatocyte misc Inosine misc Biliverdin misc Preconditioining |
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misc Torpor misc Hepatocyte misc Inosine misc Biliverdin misc Preconditioining |
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Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
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Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
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Otis, Jessica P. |
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Journal of comparative physiology |
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Journal of comparative physiology |
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Otis, Jessica P. Pike, Amanda C. Torrealba, Jose R. Carey, Hannah V. |
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Otis, Jessica P. |
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10.1007/s00360-017-1056-y |
title_sort |
hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
title_auth |
Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
abstract |
Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. © Springer-Verlag Berlin Heidelberg 2017 |
abstractGer |
Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. © Springer-Verlag Berlin Heidelberg 2017 |
abstract_unstemmed |
Abstract During the hibernation season, livers from 13-lined ground squirrels (Ictidomys tridecemlineatus) are resistant to damage induced by ex vivo, cold ischemia-warm reperfusion (IR) compared with livers from summer squirrels or rats. Here, we tested the hypothesis that hibernation also reduces damage to ground squirrel livers in an in vivo, warm IR model, which more closely resembles complications associated with traumatic injury or surgical interventions. We also examined whether protection is mediated by two metabolites, inosine and biliverdin, that are elevated in ground squirrel liver during interbout arousals. Active squirrels in spring and hibernators during natural arousals to euthermia (body temperature 37 °C) were subject to liver IR or sham treatments. A subset of hibernating squirrels was pre-treated with compounds that inhibit inosine synthesis/signaling or biliverdin production. This model of liver IR successfully induced hepatocellular damage as indicated by increased plasma liver enzymes (ALT, AST) and hepatocyte apoptosis index compared to sham in both seasons, with greater elevations in spring squirrels. In addition, liver congestion increased after IR to a similar degree in spring and hibernating groups. Microvesicular steatosis was not affected by IR within the same season but was greater in sham squirrels in both seasons. Plasma IL-6 increased ~twofold in hibernators pre-treated with a biliverdin synthesis inhibitor (SnPP) prior to IR, but was not altered by IR in untreated squirrels. The results show that hibernation provides protection to ground squirrel livers subject to warm IR. Further research is needed to clarify mechanisms responsible for endogenous protection of liver tissue under ischemic stress. © Springer-Verlag Berlin Heidelberg 2017 |
collection_details |
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container_issue |
4 |
title_short |
Hibernation reduces cellular damage caused by warm hepatic ischemia–reperfusion in ground squirrels |
url |
https://dx.doi.org/10.1007/s00360-017-1056-y |
remote_bool |
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author2 |
Pike, Amanda C. Torrealba, Jose R. Carey, Hannah V. |
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doi_str |
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up_date |
2024-07-04T01:20:10.135Z |
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|
score |
7.39983 |